Disproving muscle-tension hair loss hypotheses

[User27041995]

deleted

 

[Pey'J]

dnrd

 

[Armando Jose]

The existence of the Norwood hair loss pattern and the fact that it has not yet been possible to develop drugs that completely "cure" pattern hair loss or prevent it from occurring in the first place suggest that anatomy may play an important role in the development of hair loss.
Looking at the facial and masticatory muscles, it seems obvious at first glance that these (in combination with the galea aponeurotica) are the decisive component. However, just because a connection seems obvious at first glance does not mean that there is a connection – just as there is no connection between wearing a cap and pattern hair loss, even though a connection seems obvious at first glance.

Visualisation of the facial and masticatory muscles in the faces of men with pattern hair loss:
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Figure 1,2: Hair loss pattern and location of the facial and masticatory muscles, the galea aponeurotica and potential tension pattern (markings)

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Figure 3,4: Norwood hair loss pattern and facial and masticatory muscles

Hypothesis on the effects of muscle tension:
As can be seen in the Dissection photos (Figure 5,6), blood vessels supplying the scalp penetrate the facial and masticatory muscles. If the facial and masticatory muscles are chronically tense or hardened, this can put pressure on the blood vessels and impair blood flow. This can lead to stagnation or slowing of the blood flow. If the veins and thinner venules that carry blood away from the scalp are in particular continuously squeezed by the facial and masticatory muscles, this would lead to an accumulation of metabolic and waste products in the scalp, which may be the cause of a degeneration process that is said to lead to pattern hair loss.

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Figure 5,6: Dissection: Blood vessels that penetrate the facial and masticatory muscles (?)

This hypothesis would imply the following:

• Excessive tension of the scalp is not the cause of pattern hair loss.
• The extent of the accumulation of metabolic and waste products (the alleged cause of pattern hair loss) in a scalp region depends on the length of the supplying blood vessel squeezed by the facial and masticatory muscles and on the intensity of the squeezing of the blood vessels. The lower half of the head (including eyebrows and beard hair) is not affected by hair loss because the atrial and venous network is still too extensive up to these regions of the scalp and the extent of squeezing is not yet sufficient to produce the extent of a metabolic disorder that leads to hair loss.
• Heavy bleeding of the scalp reported by surgeons after an incision would say nothing about the quality and quantity of blood flow to the scalp if it is assumed that the problem is an obstruction to the outflow of blood from the scalp in the lower part of the head.

Disproving the Hypothesis:
The following investigations could be carried out to refute the hypothesis:

• Dissection: Review existing literature and perform targeted Dissection to show that the described mechanism of blood vessel squeezing by facial muscles and masticatory muscles does not exist or that it has no influence on the quality and quantity of blood flow to the scalp.
• Doppler ultrasound: A doppler ultrasound can be used to monitor blood flow in veins and venules and detect any changes. This non-invasive examination method uses sound waves to detect blood flow and visualise possible abnormalities such as stagnation or slowing of the blood.
• Laser Doppler flowmetry: This method makes it possible to measure the blood flow in small blood vessels. By using laser light, the speed of blood flow in the veins and venules of the scalp can be measured to detect changes or abnormalities.

Hypotheses on the cause of the chronic tension
The following 4 hypotheses show possible causes for the described chronic tension of the facial and masticatory muscles, which is assumed to be the cause of pattern hair loss.

Hypothesis A – Craniofacial development:
Simplified summary: Genetic factors and an unsuitable diet lead to poor craniofacial development. The consequences include chronically tense facial and masticatory muscles. If the skull is not developed symmetrically, for example, this can affect the position and functionality of the facial muscles. Such asymmetry can lead to certain muscles being overactive or overused, while others are underactive or weakened. The overactivated facial muscles must constantly work to compensate for the imbalances. This can lead to chronic tension and tightness.
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Figure 7: Examples of craniofacial development

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Figure 8: Effects of asymmetric craniofacial development on the function of the facial and masticatory muscles (?)

Related/original hypothesis:
https://tmdocclusion.com/home/connection-to-other-diseases-and-syndromes/hair-loss/
https://tmdocclusion.com/2018/07/14/more-on-hair-loss/

Hypothesis B – Stimulus-response pattern (conditioning):
Simplified summary: Due to interpersonal mimic and verbal interaction, humans are conditioned since birth to have their facial expressions under control so as not to provoke unwanted/wrong interpretations and associated reactions from their fellow humans. This results in a stimulus-response pattern, which results in chronic tension of the facial and masticatory muscles.

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Figure 9: Compilation to illustrate the importance of facial features as a tool for interaction and identification

Related/original hypothesis: https://open.substack.com/pub/user2...-is?r=288hhe&utm_campaign=post&utm_medium=web

Hypothesis C – Malocclusion:
Simplified summary: Malocclusion results in a continuous malposition of the lower jaw. This results in chronic tension of the masticatory muscles and parts of the mimic musculature.

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Figure 10: Chronic tension of the facial and masticatory muscles due to malocclusion (?)

Related/original hypothesis:

Hypothesis D – Skull shape:
Simplified summary: The shape or expansion of the skull leads to chronic tension in the facial and chewing muscles.

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Figure 11: Skull shape and Expansion

Disproving the Hypotheses:
It would be helpful to show how the hypotheses mentioned can be disproved and which studies would be necessary/suitable for this. If the proponents of a hypothesis are of the opinion that a disproof is not possible, they should explain why this is not possible.

Interesting ideas,....

But any theory regarding common baldness must explain the special pattern of hairloss, and the difference ocurrence between sexes, because in your case, the muscles are similar in both sexes.
Have you an explanation?

 

[Kojakjr]

This is so ridiculous. As the hairs disappear on the male skull.. the appearance changes. The DHT must not only damage the follicle, but undoubtedly cause other negative consequences. fibrosis, inflammation, calcification, etc.
Scalp tension may also be a consequence, but it’s not a primary cause. You can stand on your head all day. massage head & not grow any hair back.. Stem cell treatments may be a more fruitful area of inquiry.
It is really sad males have to go through this..

 

[Kojakjr]

It’s called aging.. Loss of fully functional stem cells..

 

[Armando Jose]

You can stand on your head all day. massage head & not grow any hair back..

But It can be a preventive method toavoid common hairloss

Possible reasons why women do not or only rarely experience pattern hair loss and the hair loss pattern is different:
- Lower muscle mass and muscle strength
- a different skin structure (men do not get cellulite)
- different skull shape

Nah, it s very similar

The hair loss pattern can be explained by the locations of the muscles, the location of the galea aponeurotica and the locations of the blood vessels. Impairment of the outflow of blood from upper scalp region A by muscle at location X leads to hair loss at scalp region A.

Also, it is very similar between sexes.

It’s called aging.. Loss of fully functional stem cells..

Moreless, not really aging but loss of stem cells is a important key, the size of dermall papilla define thickness of hair, explaining thinning hair before loss of them.

 

[randomuser1]

@User27041995 I can help with this riddle.

When the body recreates tissue (which was damaged or needs replacement for other reasons, e.g. due to chronic inflammatory processes) there are several factors which influence the decision whether new tissue is recreated fibrotic or non-fibrotic. The biggest pro-fibrotic factor is tension.

Scalp (muscle) tension is not the root cause of androgenetic alopecia. But as there is inflammation happening in androgenetic alopecia and this chronic inflammation leads to tissue destruction and recreation, the scalp tension steers the body towards fibrotic tissue generation. Thus, in the process of androgenetic alopecia, soft non-fibrotic tissue is replaced over time with fibrotic tissue.

With less tension the fibrosis would be slower and without tension there would probably barely be any fibrosis.

To simplify:
Inflammation + tension = fibrotic tissue regeneration
Inflammation without tension = soft tissue regeneration (or if not soft at least much less fibrotic)

Source (only one of many):
Wang et al.: Extracellular matrix stiffness – The central cue for skin fibrosis


Other factors which also move the needle on the fibrotic vs non-fibrotic scale:
1. Metabolic state and substrate dominance (Zhao et al.: Metabolic regulation of dermal fibroblasts contributes to skin extracellular matrix homeostasis and fibrosis)
2. Sex hormone balance (Avouac et al.: Estrogens Counteract the Profibrotic Effects of TGF-β and their InhibitionExacerbates Experimental Dermal Fibrosis)

 

[Dogchebag]

@User27041995 I can help with this riddle.

When the body recreates tissue (which was damaged or needs replacement for other reasons, e.g. due to chronic inflammatory processes) there are several factors which influence the decision whether new tissue is recreated fibrotic or non-fibrotic. The biggest pro-fibrotic factor is tension.

Scalp (muscle) tension is not the root cause of androgenetic alopecia. But as there is inflammation happening in androgenetic alopecia and this chronic inflammation leads to tissue destruction and recreation, the scalp tension steers the body towards fibrotic tissue generation. Thus, in the process of androgenetic alopecia, soft non-fibrotic tissue is replaced over time with fibrotic tissue.

With less tension the fibrosis would be slower and without tension there would probably barely be any fibrosis.

To simplify:
Inflammation + tension = fibrotic tissue regeneration
Inflammation without tension = soft tissue regeneration (or if not soft at least much less fibrotic)

Source (only one of many):
Wang et al.: Extracellular matrix stiffness – The central cue for skin fibrosis


Other factors which also move the needle on the fibrotic vs non-fibrotic scale:
1. Metabolic state and substrate dominance (Zhao et al.: Metabolic regulation of dermal fibroblasts contributes to skin extracellular matrix homeostasis and fibrosis)
2. Sex hormone balance (Avouac et al.: Estrogens Counteract the Profibrotic Effects of TGF-β and their InhibitionExacerbates Experimental Dermal Fibrosis)

How did you find this information?

 

[Renovation]

How did you find this information?

Even if the 'riddle' is correct which I believe it is party, the start of it where he says -

'Scalp (muscle) tension is not the root cause of androgenetic alopecia'

Is not addressed in the reasoning. This is a vital factor and one which imo is very wrong.

It's is blindingly obvious that deep chronic and muscle tension around the neck in particular the sternocleidomastoid muscle, will pull anything above it (with the added aid of gravity) downward. In this case the galea skin. This is a matter of fact. It may or may not also affect blood flow but that's a secondary effect.

The scalp skin itself and hence it's dermal layer is pulled down and put under tension without a shadow of a doubt.

Whether this causes the onset of the 'riddle' is clearly disputed but imo it's clear as day.

 

[Pey'J]

Even if the 'riddle' is correct which I believe it is party, the start of it where he says -

'Scalp (muscle) tension is not the root cause of androgenetic alopecia'

Is not addressed in the reasoning. This is a vital factor and one which imo is very wrong.

It's is blindingly obvious that deep chronic and muscle tension around the neck in particular the sternocleidomastoid muscle, will pull anything above it (with the added aid of gravity) downward. In this case the galea skin. This is a matter of fact. It may or may not also affect blood flow but that's a secondary effect.

The scalp skin itself and hence it's dermal layer is pulled down and put under tension without a shadow of a doubt.

Whether this causes the onset of the 'riddle' is clearly disputed but imo it's clear as day.

Not listening to saw palmetto copers

 

[Jakejr]

The scalp has 5 layers.. The hair is in the first layer.. which is the thickest layer
The galea (third layer) is almost paper thin in comparison.. It stretches across top of head to basically top of nose. It attaches in the back of head to twin occipital muscles & gets even thinner on sides of scalp.. There are multiple yellow fat deposits above the galea.. Galea is used when you raise your eyebrows..

 

[randomuser1]

Even if the 'riddle' is correct which I believe it is party, the start of it where he says -

'Scalp (muscle) tension is not the root cause of androgenetic alopecia'

Is not addressed in the reasoning. This is a vital factor and one which imo is very wrong.

Because tension alone does not explain two other things happening:
- fibrosis
- calcification


I'll extend what I said before:
Inflammation + tension = fibrotic tissue regeneration
Inflammation without tension = soft tissue regeneration (or if not soft at least much less fibrotic)
No inflammation + tension = maybe some squeezing bot no fibrotic tissue remodeling
No inflammation * no tension = super healthy scalp, no hair loss at all


Calcification usually happens as a downstream effect of vascular damage from (a) blood pressure and (b) blood glucose. As calcification happens due to internal repair mechanisms this is another indicator that external tension is not the main driver.

But yes, tension is absolutely a factor: At the very least it accelerates balding (maybe even a lot), maybe it is even a necessary co-condition for pattern hair loss to manifest.

The bigger factor is however in my opinion insulin resistance: Primary (carbs/sugars/diet) and secondary (stress, lack of sleep, diet-induced inflammation...).

I believe these two together - insulin resistance (primary or secondary) and tension explain hair loss together. See here for more.

 

[Jakejr]

The people talking about scalp tension refer to the galea- the third layer of scalp.. a very thin muscle on top of scalp & a bit on sides & upper back of skull. It may get tight.. but why does it get tight? Nobody seems to answer that question. I don’t know .. but it’s probably from Calcification. When I say calcification— I don’t mean blobs of calcium deposits— no I mean a thin layer of calcification— not enough to alarm a doctor, but just enough to restrict blood/nutrient flow to the super sensitive hair follicles. I’m currently testing a chemical which has research to back it breaking up calcification. I believe once the calculation lessens the scalp tension will also lessen..

 

[Renovation]

The people talking about scalp tension refer to the galea- the third layer of scalp.. a very thin muscle on top of scalp & a bit on sides & upper back of skull. It may get tight.. but why does it get tight? Nobody seems to answer that question. I don’t know .. but it’s probably from Calcification. When I say calcification— I don’t mean blobs of calcium deposits— no I mean a thin layer of calcification— not enough to alarm a doctor, but just enough to restrict blood/nutrient flow to the super sensitive hair follicles. I’m currently testing a chemical which has research to back it breaking up calcification. I believe once the calculation lessens the scalp tension will also lessen..

Imo the calcification fibrosis or whatever is the driving factor in scalp tension is due to the simple mechanism of extremely tight supporting inner and outer neck muscles. This along with gravity (excelled by poor posture) pulls down on the galea, which inflames the inner tissues, with this resulting inflammation causing the above.

A secondary issue with this is restricted blood flow caused by the same chronic tight deep muscles issue, and compelled again by poor posture and poor facial structure as discussed in other current threads. Of course you will still bleed a lot from the scalp, but the blood pressure is greatly reduced on arteries above the ear as opposed to below.

Several factors contribute to scalp tension, which causes the inflammation/DHT/calcification/fibrosis/ which will miniaturize hair over a long period of time.

 

[Jakejr]

Sounds good.. but what is the protocol of addressing this condition…There are plenty of arteries & their branches all through the scalp.. So there is potentially plenty of blood flow… but gradually calcifification, DHT, tension, inflammation, sebum increase…Oh so gradually so doctors don’t notice.. But we do—as hairs start to fall out.. Hairlines recede.. Density is lessened..
For me I have added direct de-Calcification to my regimen.. I’m also trying lidocaine on my forehead & eye orbitals & didn’t realize how much tension these areas are under.. Balding is a silent killer of hairs.. One thing leads to another..

 

[Renovation]

Sounds good.. but what is the protocol of addressing this condition…There are plenty of arteries & their branches all through the scalp.. So there is potentially plenty of blood flow… but gradually calcifification, DHT, tension, inflammation, sebum increase…Oh so gradually so doctors don’t notice.. But we do—as hairs start to fall out.. Hairlines recede.. Density is lessened..
For me I have added direct de-Calcification to my regimen.. I’m also trying lidocaine on my forehead & eye orbitals & didn’t realize how much tension these areas are under.. Balding is a silent killer of hairs.. One thing leads to another..

I agree, it really is trial and error. Because it takes so long for hairs to miniaturize and vice versa, it's difficult to see what's helping and what's not and patience is key.

My main aim now is to reduce neck and temporalis muscle tension and monitor scalp tension even all this is really difficult. If the main driver for the miniaturization is actually the veins carry blood away from galea, reducing the tension will have the same positive effect.

One thing which is instant is lying or sitting in a position which takes tension away, my hair feels fuller after a while, however no idea if this actually reduces scalp tension in long run yet.

I would be interested to see how the lidocaine impacts your success. I have tried to address calcification directly with AVC and disposable magnesium flakes in the past.

 

[Jakejr]

I’m trying a tablespoon of apple cider vinegar in a tumbler of water first thing in morning— also on thinning areas of scalp
& sodium thiosulfate on scalp. Both break up calcification.. I read many articles, reviews, & videos on the subject.. The problem as I study it is the scalp calcification I am talking about isn’t causing a particular health problem for doctors to zoom in on— so there are no protocols to identifying the condition & treating it.. Calcification if the tendons or shoulder can be x-rayed, can be prescribed exercises, drugs, or even surgery— where surgeons go in & pick out the calcification deposits. In the scalp (which has 5 layers) I know I have calcification because the top layer where the follicles are & which is the thicknest layer.. when I microneedle.. I can actually hear the crackling of the calcification when those sharp needles pierce the scalp.. like a saltine cracker cracking.. So I’ve done this for about a month & I see some hair regrowth.. btw I am doing other things also so one never knows exactly. I’ve studied the galea theory. Tried the massage protocol, got an electric scalp massager.. probably tried few models.. bought the scalp massage device from Hairguard I believe.. tried it for few months & then resold it. Galea is 3rd layer of scalp skin. It’s very thin compared to first layer..
So I keep experimenting..

 

[randomuser1]

Imo the calcification fibrosis or whatever is the driving factor in scalp tension is due to the simple mechanism of extremely tight supporting inner and outer neck muscles. This along with gravity (excelled by poor posture) pulls down on the galea, which inflames the inner tissues, with this resulting inflammation causing the above.

Do you have sources for supporting this? Why would tension on its own lead to inflammation and calcification? Yes, inside a muscle tension can lead to inflammation, but the issue are the hairs. Also, calcification is not explained by this.

On the other hand, there are literally dozens of studies showing that Androgenetic Alopecia is correlated with metabolic syndrome and insulin resistance:

Title	Link
Association of Androgenetic Alopecia with Metabolic Syndrome: A Case–control Study on 100 Patients in a Tertiary Care Hospital in South India	link
Early androgenetic alopecia as a marker of insulin resistance	link
Androgenetic alopecia, metabolic syndrome, and insulin resistance: Is there any association? A case–control study	link
Androgenetic alopecia as an indicator of metabolic syndrome and cardiovascular risk	link
Severe androgenetic alopecia as a maker of metabolic syndrome in male patients of androgenetic alopecia: a hospital based case control study	link
Risks for metabolic syndrome and cardiovascular diseases in both male and female patients with androgenetic alopecia	link
Study of prevalence of metabolic syndrome in androgenetic alopecia	link
Alopecia and the metabolic syndrome	link
The association of insulin resistance and metabolic syndrome in early androgenetic alopecia	link
Is early onset androgenic alopecia a marker of metabolic syndrome and carotid artery atherosclerosis in young Indian male patients?	link
Association of Androgenetic Alopecia With Mortality From Diabetes Mellitus and Heart Disease	link

Metabolic syndrome and insulin resistance, in turn, are known to cause both inflammation and calcification. The latter especially because of atherosclerosis. Summoning calcium is the body's standard response to vascular damage. And the scalp is highly vascularized. In fact, hair follicles can create their own capillaries to connect to the head's blood supply.

I am not saying that scalp tension plays no role. I think it does. The most important mechanism is that tension leads to fibrosis when inflammation is present. But what causes the inflammation (which scalp tension concerts into fibrosis) and calcification? Metabolic issues.

 

[Jakejr]

You are asking important questions…to sum up as an example — 100 patients in India who have male pattern baldness also have elevated insulin markers.. Yes.. I agree male pattern baldness is not a healthy condition.. There are 1,000 of studies finding this correlation or that correlation. I even saw a study saying drinking excess coffee leads to male pattern baldness with charts & discussion.
If you are asking specifically if scalp tension causes male pattern baldness.. I think it’s in the same category a”market” But the more important question is how did normal “galea” get stiff or manifesting tension.
As far as I know —doctors don’t measure scalp tension.. It’s subjective at this point. So for me it may be important.. but if I massage my head an hour a day.. I see no discernible results.. So at this point the jury is out.. I would prefer to think calcification stiffened the galea in the first place.. And this stiffness creates inflammation, excessive sebum, all working together to strangle the hairs/follicles.. So to say there are tetiary markers like insulin or high blood pressure.. I would submit a mineral analysis would show an imbalance in the diet of calcium, potassium, phosphorus, magnesium.. but that’s another issue..
What do we then do about it?
Like me if you are convinced calcification is the culprit you treat it.. If you think inflammation is the culprit-you treat it. If muscle tension—you treat it—if high blood pressure or insulin markers —you treat it— AND OBSERVE..
If male pattern baldness has 50 different s discernible markers soecified in medical studies— you digest what they say.. but as we all now MINOXIDIL studies said Minoxidil sulfate grew hairs 19X more than the control in the laboratory.. BUT the laboratory is not the human scalp..

 

[Renovation]

Do you have sources for supporting this? Why would tension on its own lead to inflammation and calcification? Yes, inside a muscle tension can lead to inflammation, but the issue are the hairs. Also, calcification is not explained by this.

On the other hand, there are literally dozens of studies showing that Androgenetic Alopecia is correlated with metabolic syndrome and insulin resistance:

Title	Link
Association of Androgenetic Alopecia with Metabolic Syndrome: A Case–control Study on 100 Patients in a Tertiary Care Hospital in South India	link
Early androgenetic alopecia as a marker of insulin resistance	link
Androgenetic alopecia, metabolic syndrome, and insulin resistance: Is there any association? A case–control study	link
Androgenetic alopecia as an indicator of metabolic syndrome and cardiovascular risk	link
Severe androgenetic alopecia as a maker of metabolic syndrome in male patients of androgenetic alopecia: a hospital based case control study	link
Risks for metabolic syndrome and cardiovascular diseases in both male and female patients with androgenetic alopecia	link
Study of prevalence of metabolic syndrome in androgenetic alopecia	link
Alopecia and the metabolic syndrome	link
The association of insulin resistance and metabolic syndrome in early androgenetic alopecia	link
Is early onset androgenic alopecia a marker of metabolic syndrome and carotid artery atherosclerosis in young Indian male patients?	link
Association of Androgenetic Alopecia With Mortality From Diabetes Mellitus and Heart Disease	link

Metabolic syndrome and insulin resistance, in turn, are known to cause both inflammation and calcification. The latter especially because of atherosclerosis. Summoning calcium is the body's standard response to vascular damage. And the scalp is highly vascularized. In fact, hair follicles can create their own capillaries to connect to the head's blood supply.

I am not saying that scalp tension plays no role. I think it does. The most important mechanism is that tension leads to fibrosis when inflammation is present. But what causes the inflammation (which scalp tension concerts into fibrosis) and calcification? Metabolic issues.

I don't dispute the correlation with metabolic issues but no matter how many studies are published I know or have met far to many people with type 2 diabetes and a full head of thick hair, and just as many people with incredible metabolic systems who are slick bald.

I have read things regarding muscle tension in and around the neck causing scalp inflammation as well as reducing blood flow and blood pressure towards the galea, however if we had studies on this like we do everything else hairloss related then chiropractors and physiotherapists would be making billions from male pattern baldness. Maybe in 50 years they will do.

It's trial and error for myself and controling blood sugar is something I'm currently investigation to cover another base.